Advances in Human Pathogenic Trypanosomatids

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Parasitic Pathogens".

Deadline for manuscript submissions: 31 January 2025 | Viewed by 1648

Special Issue Editor


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Guest Editor
1. Institut Pasteur de Montevideo, Montevideo 11400, Uruguay
2. Facultad de Medicina, Universidad de la República, Montevideo 11800, Uruguay
Interests: Trypanosoma cruzi; Leishmania; genomics; molecular parasitology; Chagas disease; Neospora caninum
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Special Issue Information

Dear Colleagues,

Trypanosomatids are unicellular parasites responsible for several neglected diseases, causing significant morbidity and mortality in millions of people worldwide. For example, Trypanosoma cruzi, African trypanosomes, and Leishmania spp. are responsible for Chagas disease, sleeping sickness, and various forms of leishmaniasis, respectively. These parasites have complex life cycles involving two hosts, one vertebrate and one invertebrate. Additionally, they can infect a wide variety of mammals, leading to both domestic and wild animal disease reservoirs.

Although these parasites share a common ancestor, millions of years of evolution have resulted in significant differences among them. For instance, African trypanosomes are extracellular, while Leishmania and T. cruzi invade cells for their replication, with the former targeting the mononuclear phagocytic system and the latter both professional and non-professional phagocytic cells.

A common trait among these parasites is their ability to persist within their hosts, achieved through various strategies of invasion and immune evasion. These biological characteristics present significant research challenges, necessitating diverse approaches, including the search for drugs and vaccines and understanding their invasion mechanisms, immune system modulation, and gene expression regulation, among others.

This Special Issue focuses on original research contributions and review articles on human pathogenic trypanosomatids, aiming to explore their immunological, cellular, molecular, and biochemical characteristics within the context of host–pathogen interactions and advance our understanding of their biology.

Prof. Dr. Carlos Robello
Guest Editor

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Keywords

  • trypanosomatids
  • Trypanosoma cruzi
  • African trypanosomes
  • Chagas disease
  • sleeping sickness
  • Leishmania spp.
  • leishmaniasis

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Published Papers (1 paper)

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Research

13 pages, 6875 KiB  
Article
From Trypomastigotes to Trypomastigotes: Analyzing the One-Way Intracellular Journey of Trypanosoma cruzi by Ultrastructure Expansion Microscopy
by Ramiro Tomasina, Fabiana C. González, Andrés Cabrera, Yester Basmadjián and Carlos Robello
Pathogens 2024, 13(10), 866; https://doi.org/10.3390/pathogens13100866 - 2 Oct 2024
Viewed by 1425
Abstract
The protozoan parasite Trypanosoma cruzi is the causative agent of Chagas disease, also called American trypanosomiasis. This neglected tropical disease affects millions of individuals across the Americas. To complete its life cycle, T. cruzi parasitizes both vertebrate hosts and its vector, commonly known [...] Read more.
The protozoan parasite Trypanosoma cruzi is the causative agent of Chagas disease, also called American trypanosomiasis. This neglected tropical disease affects millions of individuals across the Americas. To complete its life cycle, T. cruzi parasitizes both vertebrate hosts and its vector, commonly known as the ‘kissing bug’. The parasite’s survival and proliferation strategies are driven by the diverse environments it encounters. Despite being described by Carlos Chagas in 1909, significant knowledge gaps persist regarding the parasite’s various life forms and adaptive capabilities in response to environmental cues. In this study, we employed Ultrastructure Expansion Microscopy to explore the intricate journey of T. cruzi within the host cell. Upon entry into the host cell, trypomastigotes undergo folding, resulting in intermediate forms characterized by a rounded cell body, anterior positioning of basal bodies, and a shortened flagellum. The repositioning of basal bodies and the kinetoplast and the shortening of the flagella mark the culmination of intracellular amastigogenesis. Furthermore, we analyzed intracellular trypomastigogenesis, identifying discrete intermediate forms, including leaf-shaped stages and epimastigote-like forms, which suggests a complex differentiation process. Notably, we did not observe any dividing intracellular epimastigotes, indicating that these may be non-replicative forms within the host cell. Our detailed examination of amastigote cell division revealed semi-closed nuclear mitosis, with mitotic spindle formation independent of basal bodies. This study provides new insights into the morphological and cytoskeletal changes during the intracellular stages of T. cruzi, providing a model for understanding the dynamics of intracellular amastigogenesis and trypomastigogenesis. Full article
(This article belongs to the Special Issue Advances in Human Pathogenic Trypanosomatids)
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